Aging Integumentary System

6/28/2016
Jill Heitzman, PT, DPT
Board Certified Geriatric Clinical Specialist
Board Certified Neurologic Clinical Specialist
Certified Wound Specialist
Certified Exercise Expert for Aging Adults
Auburn, AL
FUNCTIONS OF THE SKIN
Protection:
Physical barrier to micro organisms and foreign matter to fight
against infection and excessive loss of fluids, storage of fat
and water
Sensation:
Nerve endings present in the skin allow ability to feel pain,
pressure, heat and cold
Thermoregulation: Regulates body temperature through vasoconstriction,
vasodilation and sweating
Excretion:
Excretion of waste products such as electrolytes and water
Metabolism:
Synthesis of Vitamin D in skin exposed to sunlight, activates
metabolism of calcium and phosphates; minerals important in
bone formation, Hormonal production and synthesis
Body Image:
Performs cosmetic, identification and communication roles
Immunologic:
Resident immune cells that participate in immune processing
are present in epidermis and dermis (Langerhans cells and
dermal dendritic cells, respectively)
 Over the lifespan skin becomes
 drier, less elastic
 less perfused
 vulnerable to damage from pressure, friction,
shear, moisture, malnutrition
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Appearance changes
 Skin tags, warts and other blemishes.
 Hair and nails change
Hair changes: Normal Aging
 Reduced hormone levels result
 decrease in size of the hair follicle and
thinning of the hair is noted.
 Diminished melanin results in the color
transitions to gray.
A thorough hair and scalp inspection can identify
underlying pathologies and pathologies can
impact Hair changes
Hair Changes associated with
Pathology
 Hair loss
 Alopecia: rapid loss that is patchy or diffuse
 May be associated with pharmacology or chemotherapy
 Heparin can produce hair loss
 Hair texture
 Changes indicate hypothyroidism
 Protein malnutrition can make the hair dry or course;
can also change color to a reddish or bleached
appearance
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Nail Changes
*The nail bed is very vascular and an excellent location for
assessing the adequacy of the patient’s peripheral
circulation.
 Nail beds :
 bluish or purple in color may indicate cyanosis
 pale may indicate reduced arterial blood flow.
 Decreased peripheral circulation
 Nails grow more slowly but often thicker; brittle and split into
layers.
Nail Changes
Nail changes can also indicate functional and nutritional
status:
 Mobility decline and visual changes,
 Nails appear unkempt appearance

may require podiatrist or other health care provide to reduce the
risk of surrounding skin damage and wounds.
 Nails can indicate nutritional deficiencies.
 Protein deficiency: Bands across the nail
 Zinc deficiency: White spots across the nail
 Anemia: Spoon shaped nails
 Normal aging changes skin
 80% of adults older than 65 suffer 1 or more chronic
conditions
 Drug therapies contribute to fragility of the skin
 Advanced age, comorbidities, medications,
environmental factors, nutrition and lifestyle
contribute to the overall condition of the skin
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Risk Factors affecting Aging Skin
and Wound Healing
 Age
 Stress
 Nutrition
 Bacterial
 Obesity
 Comorbidities
 Polypharmacy
 Decreased mobility
 Decreased mental status
burden/infection
 Smoking
 Pressure
 Irradiation
 Incontinence
AGE
 Age alone is not a risk factor for impaired
integumentary
 The increase in comorbidities has a greater impact
 However, some physiological changes impact function
of the integumentary system
Epidermis
 Function is for moisture retention and protection
 With aging:
 The epidermis thins
 Decrease in the density of the Langerhans Cells
 RESULTS
 Less effective in protection from infection and
dehydration
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Basement Membrane
 Functions as an interface between epidermis and
dermis and composed of projections known as rete
pegs to provide resistance to shearing forces
 With Aging:
 Rete pegs flatten leading to thinning of the basement
membrane
 RESULTS
 Increased vulnerability to shear related injury
Dermis
 The deeper layer of the skin that is responsible for:
 Structural integrity and provides nutrition, hydration and
oxygen to the epidermis via diffusion
 Composed of:


collagen which provides tensile strength
Elastin which provides ability of the skin to stretch and recoil
Dermis (cont.)
 With Aging:
 A decrease in fibroblasts leads to decrease in production
of elastin and collagen
 Collagen becomes disorganized
 Degradation of elastin fibers
 Dermis layer thins and has fewer blood vessels and
nerve endings; remaining blood vessels thin
 RESULTS
 Decreased sensation and blood supply
 The thin remaining blood vessels prone to hemorrhage

Senile Purpura: discoloration of skin
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Subcutaneous Layer
 Composed of adipose tissue, blood, and lymphatic
vessels, nerves
 Function is to facilitate regeneration of the dermis and
to connect the dermis to underlying structures
 With Aging
 Thinning of all components of subcutaneous layer
 RESULTS
 Decreased ability to provide structural protection
 Decreased thermal regulation
 Slow regeneration
Younger
Older
Epidermis
Dermis
Subcutaneous
Decrease epidermal and dermal layers
Decreased ground substance, elastin & collagen in dermis
Reduced epidermal turnover
Flattened epidermal rete pegs and dermal papillae
Decreased thickness of dermis and hypodermis
Decrease in pain perception
 Decrease number of






melanocytes
Decrease number of
Langerhans cells
Decrease mast cells
Decrease sweat glands
Diminished vascularity
Decreased subcutaneous
fat
Decrease epidermal and
dermal layers
 Decrease elastin and
collagen in dermis
 Reduced epidermal
turnover
 Flattened epidermal rete
pegs & dermal papillae
 Decrease thickness of
dermis and hypodermis
 Decrease pain perception
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Aging affects on the
Phases of wound healing
 Hemostasis
 Inflammatory
 Proliferation
 Epithelialization
 Maturation
 Inflammation phase changes
 Decrease response/migration of cells
 Prolong phase
 Proliferative phase
 Decrease amounts of fibronectin
 Excess degradation of wound bed
 Maturation phase
 Slow wound contraction/epithelialization
 Reduced tensile strength
 Altered skin permeability
 Alterations of temperature regulation/ decrease
insulation
 Increase risk for infection
 Decreased elasticity/durability of the scar
 Less scar formation
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ALTERED WOUND HEALING PROCESS
 Progressive loss of skin function
 increased vulnerability to the environment
 decreased homeostatic ability.
 The result is
 poor wound healing
 greater risk for infection
 altered inflammatory response.
 Leads to
 a breakdown of normal tissue
 impairment in acute wound healing
 predisposes the aging adult to chronic wounds.
Delayed
Slower
Increased risk for infection
Comorbidities Contributing to Skin
Alterations and Delayed Wound Healing
 Long standing chronic diseases affect wound healing due
to circulatory & nutritional deficits, mobility and
sensation issues, and multiple pharmaceutical
interventions
 Diabetes
 Vascular disease: Arterial or Venous
 Cardiac diseases
 Neurological
 Dementia/Cognition/depression
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 PVD, COPD, anemia:
 Decrease oxygen and nutrients to the wound
 Decrease bloody supply /perfusion
 Diabetes:
 Damage to WBC and macrovascular system
 Immunosuppression:
 Affects collagen synthesis during proliferation
 Limits immune cells during inflammation
 Medications/chemotherapy increases these affects….
 Neurological diseases
 Impaired mobility
 Loss of sensation
 Hematological diseases
 Anemia
 Leukemia
 Hepatic dysfunction:
 Decrease protein/albumin
 Edema
 Risk of infection
 Increase risk of dehiscence
 Faulty collagen deposition
 Alcoholism:
 Affects: nutritional status, liver, CV system and mental
status.
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Co morbidity considerations
 80% pressure ulcer-associated deaths occur in persons
over 75 years
 Controversy regarding prevention of pressure ulcers in
neurological disease and end of life
 Vicious cycle of chronic conditions leading to functional
decline, malnutrition, deconditioning and immobility
leading to open wounds which then perpetuates the cycle
 Steroids: (prednisone, cortisone)
 Decreases vascular permeability
 Has catabolic effect on peripheral tissue
 Interfere with inflammation and fibroblast growth
 Inhibits epidermal regeneration/epithelization
 Decreases tensile strength
 NSAIDS
 Topical delays re-epithelialization
 Oral reduces the inflammatory process
Medications Contributing to Skin
Alterations
 Corticosteroids
 Antibacterials
 Antihypertensives
 Analgesics
 Tricyclic antidepressants
 Antihistamines
 Antineoplastic agents
 Antipsychotic drugs
 Diuretics
 Hypoglycemic agents
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Other drug issues
 Nonsteroidal anti-inflammatory drugs (NSAIDS)
 diminished inflammatory response
 Impact is greater with those with diabetes
 Immunosuppressive agents
 affect duplicating cells.
 Warfarin
 increases bleeding tendency
 Tight control of diabetes management is needed for
wound healing
 High blood sugar





decreases the rate of collagen synthesis
decreases the rate of angiogenesis
decreases fibroblast proliferation
decrease tensile strength
inhibits re-epithelialization
 Sustained hyperglycemia decreases all phases of
healing and the body’s ability to fight infection
A1c Importance
 High blood glucose levels can lead to integumentary
trauma
 Trauma/stress can lead to high blood glucose levels
 Need to know the history of the high blood glucose
not just the current day
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FUNDAMENTAL AREA OF WOUND HEALING OFTEN
OVERLOOKED
Nutritional Status of NH patients
 232 NH patients studied by anthropometric
measurements and biochemical profiles
 59% had some form of malnutrition
 17 of those had pressure ulcers
Gruen, 2016)
Nutrition
 Ulcerations correlates to:
 Nutritional deficiencies/intake
 Undesired weight loss
 Low body mass index (<18.5)
 Wound healing increases the demand for calories and
protein with deficiencies resulting in:
 Prolong inflammatory phase
 Inhibition of fibroplasia & proteoglycan synthesis and
decrease angiogenesis (proliferative phase)
 Inhibiting remodeling
Gruen, 2016)
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Nutrition Risk
 “anorexia of aging”
 appetite decline
 weight loss
 decreased metabolic rate
 Protein-Energy Malnutrition (PEM)
Definition:
Wasting and excessive loss of lean body mass resulting
from too little energy being supplied to the body tissue
that can be reversed solely by the administration of
nutrients
Malnutrition
 Independent risk factor for increased pressure ulcers
 Correlation between malnutrition and
 Loss of taste sensation
 Poor denture
 Loss of spouse/socialization
 GI changes
 Comorbidities/pharmacology (restricted diets)
 Stressors: Recent move, recent loss, illness
Pathological State
 Imbalance between intake and body needs leads to:
 loss of body weight-10% of body wt in 6mos or 5% in 30days
 muscle wasting
 poor wound healing
 loss of skin integrity resulting in spontaneous wound
development
 development of chronic wounds and infections
 Low protein levels associated with:
 increased interstitial edema decreasing the delivery of nutrients
to the damaged tissue
 increased risk for pressure ulcers.
Diagnosis: Failure to thrive
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OBESITY
 Adipose tissue has poor blood supply
 Malnutrition is common, especially protein malnutrition,
 Operations on people who have prolonged healing times due
to:
 the prolonged operations
 greater blood loss
 decreased tissue perfusion and oxygenation
 increased intra-abdominal pressure
 immobility.
These patients, if bed ridden for any length of time, have a
greater risk for developing pressure ulcers due to easily
exceeding the capillary closing pressure of 32mmHg especially
if their body weight is superimposed over a bony prominence
OBESITY
 Increase stress on the surgical site
 Decrease tissue perfusion
 Decrease in tissue oxygenation
 Greater risk for pressure ulcers
 Vasoconstriction
 Increase in platelet aggregation
 Decrease in available oxygen
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IRRADIATION
 Radiation Therapy causes
 Cellular injury to fibroblasts, endothelial cells and
vascular supply in the area
 Can produce edema and burns
The aging process results in a delayed
healing process -up to 4x slower than
younger populations
BUT
unless another co morbid factor is
present, healing will be effective, just
slowed.
Chronic Wounds
Characterized as
 a non healing wound with prolonged
inflammation
 defective re-epithelialization,
 impaired matrix remodeling
 and/or harmful bacteria loads.
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BACTERIAL BURDEN/INFECTION
 May be systemic or local
 Result is a prolonged uncontrolled inflammation
phase
All wounds have bacteria; infection is classified as a
bacterial burden of >105 organisms/gram of tissue
Infection/antibiotics
 All chronic wounds have bacteria present
 60% of patients with chronic wounds have received
antibiotics, increasing the risk of ADR and affecting
not only wound healing but the affect of other
medications
 Move from wound contamination to colonization
needs to be identified:
 The wound will show signs of distress and appear
stalled in relation to the phases of healing.
 The infection can remain local or become systemic.
 Bacterial cells reaching a level of greater than 105/gram of
tissue is perceived to be a key determinant in infection
and delayed wound healing
Early Clinical Recognition
 Pain and tenderness may be indicative of wound infection but pain
may also present for other reasons.
 Other clinical signs of infection include
 change in quantity, color, or odor of the drainage
 presence of pus
 erythema of the wound edges
 local pain and/or edema
 increased temperature
 abnormal or absent granulation tissue
 cellulitis
 change in the periwound sensation
Acute wound infections seem to be most associated with pain,
redness, swelling, loss of function and increased temperature.
Chronic wound infections are more associated with increased pain,
wound breakdown, odor, and friable granulation tissue.
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Superficial or Deep Infection
Superficial bacterial damage will Deep infections show signs of
present with NERDS:
STONES:
Size increase
 Nonhealing

 Exudate increasing
 Temperature of periwound increases
 Red friable granulation
 Osteo structures can be probed or
 Debris on the surface
 Smell
 These superficial bacterial
infections usually treated
topically.
exposed (i.e. bone)
New areas of breakdown
 Erythema/Edema/Exudate increases
 Smell

 These deeper wound
infections need to be cultured
for proper systemic
intervention.
MRSA
 Potentially increasing due to the increase use of broad
spectrum antibiotics
 Hospital Acquired
 Tends to lead more to systemic infection
 Needs antibiotics that are out of the resistant strain
 Community Acquired
 Tends to lead more to skin and soft tissue infection
 Can be more often treated locally with topical agents
and silver impregnated dressings
Yeast/Fungi Infections
 Superficial: Tinea pedis (athlete’s foot)
 Intermediate: Candida Albicans
 Deep: Aspergillosis: invade underlying tissues
 Risk for yeast and fungal infections in aging adults:
 Antibiotics and corticosteroids
 Candidiasis
 presents in moist skin folds and appears as
erythema, a whitish pseudo membrane and
peripheral papules and pustules (cottage cheese like)
 Oral Candidiasis, thrush
 appears as a white coating of the oral cavity,
especially the tongue. This type of yeast infection
produces fissures on the tongue and restricts oral
intake, compromising the aging adult further.
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Yeast/Fungi Infections
 Candidiasis
 Presents in moist skin folds
 Appears



Erythema
Whitish pseudo membrane
Peripheral papules and pustules
 Oral Candidiasis, thrush
 White coating of the oral cavity, especially the tongue.
 Produces fissures on the tongue
 Restricts oral intake, compromising the aging adult
further.
Immobility
Leads to:
 Increase risk of pressure ulcers
 Loss of lean muscle tissue and bone density
 Decreased blood flow to the lower extremity
 Lack of use of the foot and calf pump adds to the risk
for lower extremity swelling and circulatory difficulties.
 Decreased physical activity leads to obesity and
diabetes
Incontinence
 Incontinence is not a normal part of aging
 Urinary incontinence has implications for skin
damage. Leading to maceration of the skin in this
region occurs. This will soften and separate the
epidermal layers
 A moist environment has been shown to increase the
risk of pressure ulcers
 Both urinary and fecal incontinence can alter the
skin’s integrity.
 Candidiasis often appears in the groin area further
leading to skin breakdown
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Decreased Mental Status
 Cognitive awareness is necessary for promotion of
wound healing.
 Inadequate understanding of proper nutrition or
proper skin hygiene can increase the risk of
development skin breakdown.
 Once a wound occurs, proper management includes
the cognitive factor to perform the required care for:
 wound cleansing and dressing
 skin hygiene and
 nutritional management
 medication usage (oral and topical)
 positioning for pressure or edema relief
 Dry Skin
 Rash
 Dermatitis/eczema
 Herpes
 Infections
 Skin tears
 Scars
 Cancer
 Pressure Ulcers
 Chronic Venous
Insufficiency
 Arterial Insufficiency
 Diabetes
 Skin Failure
Prevalence in Aging Adults
 Most common in those over 90 years
 Skin tears
 Venous insufficiency ulcers
 Arterial insufficiency ulcers
 Venous Leg ulcers 3-4x higher in those 80 years than
those 65-70
 Pressure ulcers 5-7x higher in those over 80 than in
those 65-70
Shah, et al, 2016
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 Major complaints of the aging population
 Supplemental additions of moisture to the skin surface
becomes necessary.
 Humidity of > 70% is required in order to draw moisture
from the environment.
 Superficial breaks occur as a result of dry skin and the
formation of deeper fissure involving the dermal base
occurs
 Excessive washing and bathing strips away the surface
lipid and induces dryness, referred to as xerosis.
 Humidifier
 Room temperature as low as comfortable
 Bathe in warm (not hot) water
 Avoid harsh soaps (those with alcohol) and drying
agents (such as powders)
 Use skin emollients (after bath while skin damp and
before bed).
 Reduce bathing frequency to 1-2 times/week
 Offering fluids to residents/patients
 Common appearance
 May indicate
 Infection
 Reaction to a pharmacological, nutrient or other
environmental intervention or contact
 Uticaria
 a raised wheal-like lesion often associated with food or
drug allergic reactions
 are often wet or oozing
 patient scratching may lead to further skin abrasions
and localized skin infections.
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 Inflammation depends on the trigger.
 The earliest and mildest skin changes seen as
Erythema & edema which may progress to
vesicles (small blisters <1cm in size).
These vesicles will begin to weep
 Followed by
 Crusts consisting of dried fluid that is either
serum (clear), pus (yellow and thick) or blood
(red-brown).
 Scaling is the end result seen on the surface of
the skin


Lesions < 1cm in size
Macule: flat
Papule: raised
Vesicle: blister
Lesions >1 cm
Patch: flat
Plaque: raised
Bulla: blister
 The chronic inflammation: skin thickening with
increased surface markings (lichenification),
excoriation, and a change in pigmentation.
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 Dry skin (xerosis)
 Hypersensitivity to allergens and other irritant
 changes in the basal epidermis & scaling.
 In the aging adult,
 Commonly seen on the hands, eyelids and ears.
 Common complaint is itching-increases at night.
 Scratching provokes the inflammatory response.
 Can also result in disfiguring skin lesions.
 Stress and environmental conditions such as foods, dust
mites, bacteria have been linked to exacerbations
 The typical skin changes in chronic venous disease.
 CVI leads to edema and capillary hyper permeability.
 Hemosiderin staining- classic pigmentation
appearance.
 The deposited fibrin leads to a woody fibrosis of the
skin
 Dryness and scaling on the legs resulting in
eczematous changes characterized by red, superficial,
itchy plaques and weepy crusts often mistaken as
cellulitis
 lipodermatosclerosis.
 Occur during the final phase of wound repair
 disorganized weave to collagen fiber bundles
 differences in capillary density
 altered pigmentation of the epidermis
 a diminished content and organization of elastic
fibers
 The tensile strength of the skin is reduced
 Affects the person’s appearance & self confidence,
especially if on the hand or face
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Documentation by:
Height, Vascularity, Pigmentation, Pliability
Active scars are raised, red, firm and pliable
Susceptible to change
Hypertrophic scars
Within boundaries of wound but
raised above surface.
Contain fibroblasts with abnormal
growth factor responses
Respond to skin substitutes & variety
of film dressings
Keloid scars
Outside the boundaries of the
wound
Appearance of a benign tumor.
Generally occur in the upper trunk,
face, neck & ears Familial, especially
in darker pigmented populations
Skin tears
 Often seen as minor inconsequential wounds, yet are very
painful and can often lead to more complications and
chronic wounds if not properly treated.
 Often there is no reported cause of the skin tear. However,
there have been links to bumping into objects, wheelchair
or bed injuries, transfers and falls.
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Skin Tears: Risks & Prevelence
 In institutions:
 Skin tears have been shown to increase during peak activity
hours of 6 to 11 AM and 3 to 9 PM.
 The risk for skin tears as a result of:
 echanical trauma when assistance is required for bathing,
dressing, toileting and transferring.
 Adhesives from wound dressings
Payne-Martin Classification System
for Skin Tears
Accepted since 1993 but has not been widely incorporated into
practice.
This classification divides skin tears into 3 categories:
Category 1: A: linear skin tear w/o tissue loss & the
epidermis & dermis are separated
B: flat w/ an epidermal flap over the dermis to w/in
1mm of wound margin.
Category 2: A: partial tissue loss of 25% of the epidermal
flap gone
B: partial tissue loss of >25% of the epidermal flap
loss
Category 3: skin tear with complete tissue loss, epidermal
flap is absent
 More common in the 6th to 8th decade.
 Usually, unidermatomal on the thoracic area
 Rare cases on the L/E associated with taking steroids
 Preceded by a mild paresthesia and pruritus within a
specific dermatome
 Contagious until the lesions have crusted
 Usually resolve in 4 weeks
 Approx. 10-20% will develop post herpetic neuralgia
 Pain that exists from 1-4 months after resolution of
the skin lesions.
 Results in sensory loss and spontaneous pain due to
destruction of sensory neurons.
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Shingles Vaccine
 CDC recommends people aged 60 and older get a
onetime vaccination
 In 2009 only 10% of this population had received the
vaccine
 By 2010, 14.4%
 In 2014, Shingles vaccine question is part of the core
questionnaire for every state to use with aging adults
 WHY??
 Shingles impacts ADLS due to intense pain, thus costs
health care dollars
 Need to adopt corrective measures to address problems
of disparities
http://www.cdc.gov/aging/pdf/state-aging-health-in-america-2013.pdf
Skin Cancer dx in 40-50% of those over age 65 at least 1x in
their lifetime, a growing global problem
Chronic vascular ulcers can degenerate into a malignancy
(Marjolin’s ulcer) and many epidermal cancers can mimic
venous ulcers in appearance, location and symptoms.
Further eval. is needed when there is:
 An increase size despite appropriate treatment
 Increase in pain
 hypertrophic (excess) granulation tissue
 Develop irregular base or margin
 Wounds with excessive bleeding
 Any deposit that has a caviar appearance
 Any change in an existing growth or a new growth on
the skin that ulcerates but does not heal as anticipated
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Asymmetry of one half of the mole not matching the
other half
Border being irregular with ragged or notched edges
Color of brown, tan or black in varying degrees but
uniform within the mole
Diameter being >6mm or the size of a pencil eraser tip
are classic signs of potential melanoma.
**There is now an additional evaluation level of
“E” for the evolution, enlargement or elevation of a
lesion
Cancer
 Skin cancer is estimated to be diagnosed in 40-50% of
those over the age of 65 at least once in their lifetime and is
a growing global problem
 The link between UV exposure and skin cancer has been
well established and induces all 3 major forms of skin
neoplasms; basal cell carcinoma, squamous cell carcinoma
and malignant melanoma.
 Chronic vascular ulcers can degenerate into a malignancy
(Marjolin’s ulcer) and many epidermal cancers can mimic
venous ulcers in appearance, location and symptoms.
Clark Staging System
 Used for determining treatment intervention.
Stage 0: A nonmelanoma lesion confined to
the epidermis.
Stage 1: Carcinomas <2cm
Stage 2: Carcinomas >2 cm
Stage 3: Involves structures below the skin,
i.e.., muscle/bone/cartilage/lymph nodes
Stage 4: Metastasized lesions
*The actual depth may vary depending upon the region
of the body involved
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Types of Skin Cancer
 Precancerous actinic keratosis
 abnormal changes in keratinocytes and can become
squamous cell carcinoma.
 Clinical features include single or multiple dry scaly
adherent lesions on habitually sun exposed skin
 usually begin as barely perceivable rough spots of skin
(sandpaper feeling); more often felt than seen
 progressing to erythematous, scaly plaques that flake of
or are exfoliated by toweling after a shower or shaving
Basal cell and squamous cell
carcinoma
 Grouped as nonmelanoma skin cancers
 The recognized cause is prolonged and cumulative
exposure to the sun
 Can be found in chronic non healing ulcers that
appear similar to other types of ulcers (venous/arterial
insufficiency, diabetic or pressure ulcers) however they
do not appear in the more typical locations.
 Often is only diagnosed after several months when
inflammatory changes and edema was improved, but
the wound was enlarged and many times having a
raised granulated edge
Basal Cell Carcinoma
 Slow growing
 Rarely metastasize
 Can cause local skin destruction and changes in
skin and body appearance
 They appear as lesions with pearly borders,
depressed centers and rolled edges
 Chronic wounds will have
 a shiny, translucent surface
 typically have uniform abundance or exuberant
granulation tissue extending above or even
overlapping the wound margins
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Squamous Cell Carcinoma
Besides UV rays, radiation and tissue damage from
scars, ulcers and fistulas may also produce
squamous cell carcinomas
 These tumors affect the skin and mucous
membranes can be more invasive and malignant
than basal cell carcinoma if not treated promptly
 Squamous cell carcinoma has a
 hyperkeratotic appearance
 may ulcerate and bleed.
 This should be suspected in a reddish/black non
healing wound that has an appearance of caviar.

Malignant Melanoma
 Highly metastatic lesions
 Worldwide, this type of cancer is growing faster than
any other except for lung cancer
 Due to chronic sun exposure, the risk for malignant
skin cancer increases with age
 Risk factors include fair complexion with a tendency to
easily sunburn and a family history of melanoma.
 The most common locations are on the legs of women
and trunk of men.
 These tumors have irregular borders, can be brown or
black and are usually larger than 6mm.
Melanoma: Breslow Depth Scale
Stage
Depth
Depth of tissue involvement
I
< 0.75 MM
Confined to epidermis
II
0.75-1.55mm
Invasion into the papillary dermis
III
1.51-2.25mm
Fills papillary dermis and compresses
the reticular dermis
IV
2.25-3.0 mm
Invasion of reticular dermis
(localized)
V
>3.0mm
Invasion of subcutaneous tissue
(regionalized by direct extension)
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Pressure Ulcers
 Pressure ulcers can reduce the overall quality of life
because of the pain, treatment interventions, and
increased length of institutional stay even
contributing to premature mortality.
 The estimated cost for pressure ulcer care:
 $11 billion annually
 $500-$70,000.oo per individual pressure ulcer
NPU Advisory Panel, 2015
 Litigations regarding pressure ulcers have also
added a financial burden on healthcare costs.
Prevalence/incidence
 Despite awareness of prevention, pressure ulcer
development continues to be a concern.
 Hospitalized patients in the United States between 1993-
2008 had a 63% increase of pressure ulcers
 The prevalence of pressure ulcers is widespread across all
settings:
 0.4-38% in acute care,
 2-24% in long-term care
 0-17% in home care.
 The incidence of new pressure ulcers is also widespread
 6% in 2008
 5% in 2009
US Dept. Of Health Human Services,2013
Friction/Shear
 The role of friction/shear is described in terms of poor
lifting and handling techniques
 Friction:
 Dragging the patient instead of lifting and increases in areas
of moisture.
 Shear:
 Patient sliding causing superficial to slide across the deeper
tissue resulting in a shearing force
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Pressure ulcers can
occur from any
pressure source
Pressure Ulcers
Characteristics
 Due to pressure
 Over bony prominence
 Vary in depth
 Necrotic tissue often present
 Exudate common
 May be painful
 Associated with malnutrition
Staging Pressure INJURY
 New staging system as of 2016
 Pressure injuries are staged to indicate the extent of
tissue damage
 Definition:
 Localized damage to the skin and/or underlying soft
tissue over a bony prominence or related medical or
other device.
 Can present as intact skin or open ulcer and may be
painful
 Occurs as result of intense or prolong pressure or in
combination with shear
 May be affected by microclimate, nutrition, perfusion,
co-morbidities, and conditions of the soft tissue
NPU Advisory Panel, 2016
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Stage 2:
Partial Thickness skin loss; exposed dermis
 Wound bed is viable, pink or red, most and may
present as an intact or ruptured blister
 Adipose tissue and deeper tissues are not visible
 Granulation tissue, slough or eschar are not present
 Often result of microclimate changes and shear over
pelvis and heel.
 Do not use to describe moisture related damage due to
incontinence, dermatitis, adhesives or trauma (skin
tears, burns abrasions)
Stage 3:
Full thickness skin loss
 Adipose is visible
 Granulation and epibole (rolled edges) often present
 Slough and/or eschar may be present
 Depth varies by anatomical location
 Undermining and tunneling may occur
 Fascia, muscle, tendon, ligament, cartilage and/or
bone is NOT exposed
 If slough or eschar obscures the extent of tissue loss
this is an Unstageable Pressure Injury
Stage 4:
Full thickness skin and tissue loss
 Exposed or directly palpable fascia, muscle, tendon,
ligament, cartilage and/or bone
 Epibole, undermining, tunneling may occur
 Depth varies by anatomical location
 If slough or eschar obscures the extent of tissue loss
this is an Unstageable Pressure Injury
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Unstageable Pressure Injury:
Obscured skin and tissue loss
 Full thickness skin and tissue loss cannot be confirmed
due to being obscured by slough or eschar
 Once removed, a Stage 3 or 4 will be revealed
 Stable eschar (dry, adherent, intact without erythema or
fluctuance) on an ischemic limb or the heel(s) should
not be removed.
Deep Tissue Injury:
Persistent non blanchable deep red,
maroon, or purple discoloration
 Intact or non intact skin or epidermal skin separation
revealing a dark wound bed or blood filled blister
 Pain & temperature changes often precede skin color
changes
 Discoloration may appear differently in dark pigmented
skin
 Results from prolong or intense pressure and shear forces
at bone-muscle interface
 May evolve rapidly to reveal actual extent of injury or may
resolve without tissue loss
Other Pressure Injuries
 Mechanical Device:
 Use of devices designed and applied for diagnostic or
therapeutic purposes.
 Injury generally conforms to the pattern or shape of the
device
 Use the staging system for documentation
 Mucosal Membrane Pressure Injury
 Injury is found on mucous membranes with history of a
medical device use in the location of the injury
 These injuries cannot be staged
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Chronic Venous Insufficiency
 Most common cause of leg ulcers;
 81% of all cases with the risk of ulcers increasing with age
 Risk increases with:
 Age
 Greater in the long term care population
 Idenified as:
 Venous hypertension >90mmHg resulting in
frequent/constant ulceration
Chronic Venous Insufficiency
 Physiological process for ulcerations:
 Edema physically stretches the skin causing
epidermal/dermal damages-resultant skin barrier
disruption.
 Skin Barrier disruption compounds the inflammatory
reaction of the underlying tissues creating more
edema worsening the epidermal damage.
 The skin may become hypersensitive to chemicals and
allergens causing more damage to the surrounding
tissues
Venous Ulcers
Characteristics
 Due to inadequate return of venous blood
 Superficial (dermal)
 Ruddy, granular tissue
 Irregular wound margins
 Leg dark, brownish hue
 Exudate usually present
 Achy pain
 Associated with venous disease
 Occur in lower leg
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Venous Wounds Classification (1-3)
 CEAP classification system consists of 4 elements:




Clinical classification
Etiologic classification
Anatomic classification
Pathophysiology
Venous Ulcer Treatment
 Treatment is restoration of venous return and
management of edema
 Elevation
 Wrapping
 Protection from injury
 Lifelong compression therapy
Arterial Insufficiency
 Have also been called ischemic ulcers and occur in
patients with peripheral artery disease (PAD)
 The primary risk factors









Diet
Hypertension
Hyperlipidemia
Hypertriglyceridemia
Diabetes mellitus
Obesity from a sedentary lifestyle
Stress
Cigarettes
Family history
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Arterial Insufficiency Ulcers
Characteristics
 Due to lack of arterial blood flow
 Deep, “punched out”
 Pale wound bed
 Leg cool, pulseless
 Necrotic tissue from embolus
 Minimal exudate
Arterial Insufficiency Ulcers
 Even wound margins
 Cellulitis common
 Associated with PVD
 Usually painful, in absence of neuropathy
 Treatment is restoration of arterial flow if
surgical candidate
Diagnostic tests:
 Ankle/Brachial index
(BP of ankle divided by highest BP of arm)
Patients with <.45 are not going to heal. At risk if <.8
Capillary refill time
Count “1001” …after pinching great toe to check
refill time.
Rubor of Dependency
Legs are pale with elevation and increase redness with
dependency
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Ankle Brachial Index
 Utilizing a Doppler for evaluating the ABI is the
preferred method
 Method:
 Patient should lay supine for 15-20 minutes prior to
measurement
 Measure both UE and take highest systolic
measurement
 For Each LE: determine the highest systolic pressure
between dorsal pedis and post tibialis
 Divide the LE systolic by the highest UE systolic
Ankle Brachial Index
 Adequate blood supply: > 0.6 and <1.2
 Borderline PAD, needs further eval: >0.6 and <0.8
 A false elevation of the ABI (>1.2)can occur in
patients with calcified vessels such as diabetes
 Elevation and compression therapy is
contraindicated in patients with arterial ulcers
especially if the ABI is less than 0.5.
Diabetes
 Microvascular or macrovascular complications can
lead to bruises or injuries that do not heal,
gangrene, and ultimately progress to amputation
 Greater risk of developing repetitive ulcerations and
infections due to the vascular changes
 Early identification of sensory loss with proper
intervention could lead to a decrease in the number
of wounds in this population.
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Neuropathic (Diabetic) Ulcers
Characteristics









Due to pressure in numb areas, such as feet
Associated with diabetes
Deep
Painless (leg neuropathic)
Even wound margins
Callous surrounding ulcer
Granular tissue, unless PVD
Cellulitis or osteomyelitis common, MRSA common
Occur on metatarsal heads, areas where shoes rub
Staging Systems for Diabetic Wounds
(Grade 0-III)
 University of Texas Diabetic Wound Classification System
(Grade 0 – III)
 0= Preulcerative or postulcerative lesion, completely
epithelialized
 I = Superficial wound, not involving tendon, capsule or
bone
 II = Wound penetrating to tendon or capsule
 III = Wound penetrating to bone or joint
Podiatrists use the Wagner Scale 0-5
0-Pre-ulcerative lesion, healed ulcers, presence
of bony deformity
1-Superficial ulcer without subcutaneous tissue
involvement
2-Penetration through the subcutaneous tissue,
may expose bone, tendon, ligament of the joint capsule
3-Osteitis, abscess or osteomyelitis
4-Gangrene of digit
5-Gangrene of the root requiring disarticulation
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The LEAP Risk scale is also used.
 Risk Category 0: Intact protective sensation
Yearly follow-up foot screening
Proper footwear education
 Risk Category 1: Loss of protective sensation (LOP),
no foot deformity
Follow-up every six months
Patient education
LEAP
Risk Category 2: LOP with foot deformity
Follow-up every three months
Patient education and skin care
Risk Category 3: LOP with foot deformity and
history of previous ulceration
or amputation
Follow-up monthly
Patient education and skin care
Custom molded orthotics
Prescription footwear
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Plus dorsal area of between 1st and 2nd distal metatarsal
Modified from Northcoast Medical
Treatment of
Diabetic(neuropathic) Ulcers
 Treatment
 Removal of callous
 Offloading
 Boots
 Shoes
 Assessment for osteomyelitis
 MRSA common
 Topicals must be selective for MRSA
***Osteomyelitis is a common complication:
Majority of amputations are preceded by this
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Skin Failure
 Langemo and Brown define “skin failure” as an
event in which the skin and underlying tissue die
due to hypo perfusion that occurs concurrent with
sever dysfunction or failure of the organ systems.
Skin Barrier Failure
 The skin is the largest organ of the body
 As with other internal organs the skin
fails too
 Acute, chronic or end-stage skin failure
Skin Deterioration
 In the failing individual, skin deterioration
is the often the most outward manifestation
of overall faltering physiology
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Acute Skin Failure
 Acute skin failure:
 Skin & underlying tissue die due to
hypoperfusion concurrent with a critical illness
 More often seen in ICU or acute care settings
Chronic Skin Failure
 Skin & underlying tissue die due to hypoperfusion
concurrent with ongoing, chronic disease states
 Occurs in a more steady fashion
 Individuals usually older and have multiple comorbidities
 Internal organ systems increasingly and irreversibly lose
their ability to function as the end of life nears
Chronic Skin Failure
Risk Factors
Manifestations
 Chronic illness
 Loss of fat & muscle mass
 Older population
 Decreased mobility
 Multiple co-morbidities
 Skin & underlying tissue
changes
 Decline in mentation
 Decreased functional
ability
 Malnutrition
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Interventions for Chronic Skin Failure
 Well documented multidisciplinary interventions
 Nutritional support
 Hydration
 Medical management
 Hygiene
 Functional rehabilitation
 Pressure redistributing surface selection
End-Stage Organ Decompensation & Failure
 Large and unusual presentations of skin failure
 Body shunts blood to vital organs
 Widespread deep tissue destruction over stressed
areas can appear in a matter of hours or less
 Sacrum
 Heels
 Posterior calf muscles
 Arms
 Elbows
Multiple Organ Death
 Reveals itself on the external skin
 Few interventions can lessen the external skin
damage as the body actively begins to shut
down
 Clear, honest communication of medical
assessments and prognosis among:
 Health care providers
 Patient/resident
 Significant others
 Establish realistic goals for treatment of
unavoidable complications, pain and suffering at
the end stages of life
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SCALE
 Skin Changes At Life’s End
 Expert panel published paper in 2008
 Current understanding of complex skin changes at
life’s end limited
 Not all pressure ulcers are avoidable
End of Life
Phase of life when a person is
living with an illness that will
often worsen and may eventually
cause death
Kennedy Terminal Ulcer
 An unavoidable ulcer
 Those who exhibit this ulcer will be at the end
stage of life
 Usually appears about 2 to 6 weeks before death
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Kennedy Terminal Ulcer
 Not a cause of a patient's death
 May starts out superficially as a blister or a Stage 2
 Looks much like an abrasion with small black almost
vasculitic spots
 Rapidly progresses to a Stage III or a Stage IV
 On sacrum in the shape of a pear, butterfly or
horseshoe with irregular borders
 Cause remains unknown
Dialogue Necessary in
Presence of Chronically Ill
 The occurrence of skin failure in the
chronically ill is a time to establish
dialogue
 Pros and cons of future aggressive
medical interventions
Should this be Palliative Care?
“The decision to move a patient from curative to a
palliative treatment plan requires that the clinician has
determined that the wound is ultimately non-healing
rather than undertreated”
Shah, 2016
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CONSIDERATIONS
Patient preference
Respect their autonomy to accept or
reject treatment
Beneficence
The best interest of the patient and
health of society
Nonmaleficence
Duty to do no harm to the patient
Justice
Impartiality/fairness
Surrogate Decision
Maker
If patient is not competent then
advance directive followed before
durable power of attorney
Patient/Family conferences:
S-P-I-K-E-S protocol
SETTING
Quiet setting, sitting eye to eye
PERCEPTION
Ask what they know about the
condition
INVITATION
Ask how much detail they want to
know
KNOWLEDGE
Present in a non technical/ simple
language in small pieces
EMOTION/EMPATHIZE/ Listen for emotion and identify
EVALUATE
cause
SUMMARIZE
Goals for Palliative Wound Care
 Preventing wound from getting larger
 Prevent new pressure ulcers
 Prevent infection
 Managing odor, exudate, bleeding
 Assessing and treating pain
 Self image, dignity, quality of life
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Practical Pointers for Palliative Care
 Practice meticulous skin care
 Avoid soap
 Use a low pH-balanced cleanser, gently
 Apply moisturizers
 Use low pH skin cleanser when incontinence
present
 Apply a moisture barrier
 Protect skin from maceration
Practical Pointers for Palliative
Wound Care
 Nutrition and hydration
 Encourage repositioning to the extent possible
 Encourage turning and repositioning if possible
 Protect heels
 Assess, treat, reassess wound associated pain
 Medications
 Appropriate wound care



Nonadherent dressings that can stay on for several days
Skin sealants
Nonpharmacological techniques
Practical Pointers for Palliative
Wound Care
 Prevent infections
 Minimize/mask odor
 Minimize or eliminate friction/shear forces
 Minimal mechanical force during wound
cleansing
 Autolytic/enzymatic debridement
preferred if needed
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Wounds at end of life
 Limited studies related to end-of-life wounds
 End-of-life wounds prevalence for ~1-million
hospice patients
 Millions of other frail elderly persons living with
chronic diseases suffer with end-of-life wounds
 Awareness of residents at risk for skin failure
 A wound/skin care program that addresses
palliative treatment can significantly enhance the
quality of life for patients/residents
Determining the Etiology of any
open wound is a critical first step
Essential Elements
 Wound assessment
 Nutrition
 Debridement
 Management of
 Cleansing
 Dressings
 Offloading
infection
 Protection from
pressure
 Documentation
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Essential Elements
 Site:
 exact location
 Stage, if pressure ulcer
 Periwound:
 color, edema, injury,
pain, warmth, texture,
maceration
 Tunneling, sinus tract,
undermining:
 location, depth
 Pain
 Size:
 length, width, depth
 Type of tissue:
 slough, necrotic,
epithelial, granulation
 Exudate:
 color, amount, odor
Pain Management
 Factors contributing to Pain
***Dried out dressings
Adherent dressings
Adhesive dressings
Wound cleansing
Wound debridement
Patient’s previous experience
Fear of hurting
Packed gauze
When is Pain Experienced?
 During Dressing removal
 During wound Debridement
 During Dressing Application
 While dressing is in wound
 Other
65%
25%
3%
2%
2%
-Moffatt et al, 2002
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Chronic Wound Pain
Persistent pain when nothing is
being manipulated.
Clinical Practice Guidelines
-NPUAP
 Document pain:
 During turning
 Dressing changes
 Debridement
 Manage pain by:
 Covering wounds
 Adjusting support surfaces
 Repositioning
 Appropriate Analgesics as needed
Effective Pain management
 Proper assessment
 Appropriate dressing selection
 Appropriate pressure relieving surfaces
 Appropriate Physical Therapy Interventions
 Patient Centered approach
 Observe body language and nonverbal cues
 Encourage deep, rhythmic breathing
 Negotiate a signal for “time out”
 Guided Imagery
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 No single dressing can provide optimum environment
for healing all wounds.
 Proper dressing can reduce medications needed for pain
 Considerations:
Use:
Types:
Absorption
Protection
Debridement
Promotion of
granulation/w
ound closure
Length before
changing:
Transparent films Daily
Hydrocolloids
3-10 days
Hydrofibers
As drainage indicates
Hydrogels
Alginates
Collagens
Foam
gauze
Modalities and Interventions
 Debridement
 Autolytic
 Enzymatic
 Sharp/Surgical
 Mechanical

 Negative Pressure Wound
Therapy
 Electrical Stimulation
 Ultrasound
 Hyperbaric Oxygen
Wet to dry, pulsatile

lavage, low frequency US,
whirlpool
Light therapy
 Biological
 Chemical
Conclusion
 Skin’s loss of integrity due to internal and external
insults that need to be recognized in order to develop
proper POC
 The Plan of Care is dependent on goals of therapy:
 Healing
 Palliative
 Restorative
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REFERENCES
 AHQR, US Dept. HHS. Pressure Risk Assessment and
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http://effectivehealthcare.ahrq.gov/index.cfm/search-forguides-reviews-andreports/?productid=1490&pageaction=displayproduct
 National Pressure Ulcer Advisory Panel.
http://www.npuap.org/news/
 Robert L; Labat-Robert J; Robert AM. Physiology of skin aging.
Clin Plast Surg. 2012; 39(1):1-8.
 Posthauer ME, Banks M, Dorner B, Schols J. The Role of
Nutrition for Pressure Ulcer Management: National Pressure
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 Sha P, Han Aung T, Ferguson R, Ortega G, Shah J. Ethical




Considerations in Wound Treatment of the Elderly Patient.
Journal of the American College of Clinical Wound Specialists,
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Gruen D. Wound Healing and Nutrition: Going Beyond Dressings
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Hakim, E.W., Heitzman, J. (2013). Wound management in the
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
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
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